TUESDAY, Oct. 13 (HealthDay News) -- Suppression of phosphoinositide 3-kinase activity in genetically-altered mice preserves cardiac function and prevents the appearance of other markers of cardiac aging, according to a study published online Oct. 12 in Circulation.

Yasutaka Inuzuka, M.D., of Kyoto University in Japan, and colleagues assessed the mechanisms of cardiac aging by analyzing and comparing age-associated changes in the hearts of genetically-altered mice with cardiac-restricted phosphoinositide 3-kinase activity and littermate mice that were non-transgenic. Cardiac function in both groups was assessed using cardiac catheterization under dobutamine infusion, and mice were euthanized at 3 months of age and 20 to 24 months for direct cardiac examination.

Cardiac functional reserve was found to be better in the old genetically-altered mice than in the old non-transgenic mice. In the old non-transgenic mice, the researchers observed an accumulation of ubiquitinated protein and lipofuscin, as well as evidence from gene expression profiling suggesting that dysregulation of protein quality characterizes cardiac aging. Among the genetically-altered mice, inhibition of phosphoinositide 3-kinase activity appeared to preserve cardiac function, prevent lipofuscin accumulation, and reduce the appearance of markers of cellular senescence.

"Suppression of phosphoinositide 3-kinase prevented many age-associated changes in the heart and preserved cardiac function of aged mice," the authors write.

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